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Long pentraxin 3: experimental and clinical relevance in cardiovascular diseases.

Bonacina F, Baragetti A, Catapano AL, Norata GD - Mediators Inflamm. (2013)

Bottom Line: Studies addressing the potential physiopathological role of CRP in the cardiovascular system were so far inconclusive and have been limited by the fact that the sequence and regulation have not been conserved during evolution between mouse and man.While PTX3 deficiency is associated with increased inflammation, cardiac damage, and atherosclerosis, the overexpression limits carotid restenosis after angioplasty.These observations point to a cardiovascular protective effect of PTX3 potentially associated with the ability of tuning inflammation and favor the hypothesis that the increased levels of PTX3 in subjects with cardiovascular diseases may reflect a protective physiological mechanism, which correlates with the immunoinflammatory response observed in several cardiovascular disorders.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacological and Biomolecular Sciences, Università Degli Studi di Milano, 20133 Milan, Italy.

ABSTRACT
Pentraxin 3 (PTX3) is an essential component of the humoral arm of innate immunity and belongs, together with the C-reactive protein (CRP) and other acute phase proteins, to the pentraxins' superfamily: soluble, multifunctional, pattern recognition proteins. Pentraxins share a common C-terminal pentraxin domain, which in the case of PTX3 is coupled to an unrelated long N-terminal domain. PTX3 in humans, like CRP, correlates with surrogate markers of atherosclerosis and is independently associated with the risk of developing vascular events. Studies addressing the potential physiopathological role of CRP in the cardiovascular system were so far inconclusive and have been limited by the fact that the sequence and regulation have not been conserved during evolution between mouse and man. On the contrary, the conservation of sequence, gene organization, and regulation of PTX3 supports the translation of animal model findings in humans. While PTX3 deficiency is associated with increased inflammation, cardiac damage, and atherosclerosis, the overexpression limits carotid restenosis after angioplasty. These observations point to a cardiovascular protective effect of PTX3 potentially associated with the ability of tuning inflammation and favor the hypothesis that the increased levels of PTX3 in subjects with cardiovascular diseases may reflect a protective physiological mechanism, which correlates with the immunoinflammatory response observed in several cardiovascular disorders.

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Related in: MedlinePlus

PTX3 as a marker of cardiovascular inflammation. A variety of cell types produce PTX3 in response to pro- and anti-inflammatory signals. Increased PTX3 levels are useful as a marker of different cardiovascular diseases including (a) cardiac inflammatory disorders, such as HF, MI, and atrial fibrillation, and (b) vascular damage, as IMT, PCI, and restenosis.
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fig2: PTX3 as a marker of cardiovascular inflammation. A variety of cell types produce PTX3 in response to pro- and anti-inflammatory signals. Increased PTX3 levels are useful as a marker of different cardiovascular diseases including (a) cardiac inflammatory disorders, such as HF, MI, and atrial fibrillation, and (b) vascular damage, as IMT, PCI, and restenosis.

Mentions: Following myocardial infarction (MI), PTX3 plasma levels peak within 7.5 hours as compared to CRP which peaks around 50 hours [13]. In MI patients, PTX3 but not CRP, after adjustment for major risk factors and other acute phase proteins, independently predicted 3-month mortality [80]. These data, suggesting PTX3 as a strong prognostic marker of CVD death, paved the road for several studies addressing its role as a biomarker of cardiovascular inflammation (Figure 2) independently of other acute phase proteins such as CRP.


Long pentraxin 3: experimental and clinical relevance in cardiovascular diseases.

Bonacina F, Baragetti A, Catapano AL, Norata GD - Mediators Inflamm. (2013)

PTX3 as a marker of cardiovascular inflammation. A variety of cell types produce PTX3 in response to pro- and anti-inflammatory signals. Increased PTX3 levels are useful as a marker of different cardiovascular diseases including (a) cardiac inflammatory disorders, such as HF, MI, and atrial fibrillation, and (b) vascular damage, as IMT, PCI, and restenosis.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3649691&req=5

fig2: PTX3 as a marker of cardiovascular inflammation. A variety of cell types produce PTX3 in response to pro- and anti-inflammatory signals. Increased PTX3 levels are useful as a marker of different cardiovascular diseases including (a) cardiac inflammatory disorders, such as HF, MI, and atrial fibrillation, and (b) vascular damage, as IMT, PCI, and restenosis.
Mentions: Following myocardial infarction (MI), PTX3 plasma levels peak within 7.5 hours as compared to CRP which peaks around 50 hours [13]. In MI patients, PTX3 but not CRP, after adjustment for major risk factors and other acute phase proteins, independently predicted 3-month mortality [80]. These data, suggesting PTX3 as a strong prognostic marker of CVD death, paved the road for several studies addressing its role as a biomarker of cardiovascular inflammation (Figure 2) independently of other acute phase proteins such as CRP.

Bottom Line: Studies addressing the potential physiopathological role of CRP in the cardiovascular system were so far inconclusive and have been limited by the fact that the sequence and regulation have not been conserved during evolution between mouse and man.While PTX3 deficiency is associated with increased inflammation, cardiac damage, and atherosclerosis, the overexpression limits carotid restenosis after angioplasty.These observations point to a cardiovascular protective effect of PTX3 potentially associated with the ability of tuning inflammation and favor the hypothesis that the increased levels of PTX3 in subjects with cardiovascular diseases may reflect a protective physiological mechanism, which correlates with the immunoinflammatory response observed in several cardiovascular disorders.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacological and Biomolecular Sciences, Università Degli Studi di Milano, 20133 Milan, Italy.

ABSTRACT
Pentraxin 3 (PTX3) is an essential component of the humoral arm of innate immunity and belongs, together with the C-reactive protein (CRP) and other acute phase proteins, to the pentraxins' superfamily: soluble, multifunctional, pattern recognition proteins. Pentraxins share a common C-terminal pentraxin domain, which in the case of PTX3 is coupled to an unrelated long N-terminal domain. PTX3 in humans, like CRP, correlates with surrogate markers of atherosclerosis and is independently associated with the risk of developing vascular events. Studies addressing the potential physiopathological role of CRP in the cardiovascular system were so far inconclusive and have been limited by the fact that the sequence and regulation have not been conserved during evolution between mouse and man. On the contrary, the conservation of sequence, gene organization, and regulation of PTX3 supports the translation of animal model findings in humans. While PTX3 deficiency is associated with increased inflammation, cardiac damage, and atherosclerosis, the overexpression limits carotid restenosis after angioplasty. These observations point to a cardiovascular protective effect of PTX3 potentially associated with the ability of tuning inflammation and favor the hypothesis that the increased levels of PTX3 in subjects with cardiovascular diseases may reflect a protective physiological mechanism, which correlates with the immunoinflammatory response observed in several cardiovascular disorders.

Show MeSH
Related in: MedlinePlus